Data extracted from this reference:

inhibition or RNA interference ablation of aldose reductase suppresses lipopolysaccharide-stimulated production of nitric oxide and over-expression of inducible nitric oxide synthase. Inhibition also prevents the lipopolysaccaride-induced apoptosis, cell cycle arrest, activation of caspase-3, downregulation of Bcl-xl and up-regulation of Bax and Bak in macrophages

Mus musculus

Inhibitors

Inhibitors

Commentary

Organism

Structure

sorbinil

inhibition of aldose reductase suppresses lipopolysaccharide-stimulated production of nitric oxide and over-expression of inducible nitric oxide synthase. Inhibition also prevents the lipopolysaccaride-induced apoptosis, cell cycle arrest, activation of caspase-3, downregulation of Bcl-xl and up-regulation of Bax and Bak in macrophages

Mus musculus

Tolrestat

inhibition of aldose reductase suppresses lipopolysaccharide-stimulated production of nitric oxide and over-expression of inducible nitric oxide synthase. Inhibition also prevents the lipopolysaccaride-induced apoptosis, cell cycle arrest, activation of caspase-3, downregulation of Bcl-xl and up-regulation of Bax and Bak in macrophages

Mus musculus

zopolrestat

inhibition of aldose reductase suppresses lipopolysaccharide-stimulated production of nitric oxide and over-expression of inducible nitric oxide synthase. Inhibition also prevents the lipopolysaccaride-induced apoptosis, cell cycle arrest, activation of caspase-3, downregulation of Bcl-xl and up-regulation of Bax and Bak in macrophages

Mus musculus

Organism

Organism

Primary Accession No. (UniProt)

Commentary

Textmining

Mus musculus

-

-

-

Source Tissue

Source Tissue

Commentary

Organism

Textmining

RAW-264.7 cell

inhibition or RNA interference ablation of aldose reductase suppresses lipopolysaccharide-stimulated production of nitric oxide and over-expression of inducible nitric oxide synthase. Inhibition also prevents the lipopolysaccaride-induced apoptosis, cell cycle arrest, activation of caspase-3, downregulation of Bcl-xl and up-regulation of Bax and Bak in macrophages

Mus musculus

-

Engineering (protein specific)

Amino acid exchange

Commentary

Organism

additional information

inhibition or RNA interference ablation of aldose reductase suppresses lipopolysaccharide-stimulated production of nitric oxide and over-expression of inducible nitric oxide synthase. Inhibition also prevents the lipopolysaccaride-induced apoptosis, cell cycle arrest, activation of caspase-3, downregulation of Bcl-xl and up-regulation of Bax and Bak in macrophages

Mus musculus

Inhibitors (protein specific)

Inhibitors

Commentary

Organism

Structure

sorbinil

inhibition of aldose reductase suppresses lipopolysaccharide-stimulated production of nitric oxide and over-expression of inducible nitric oxide synthase. Inhibition also prevents the lipopolysaccaride-induced apoptosis, cell cycle arrest, activation of caspase-3, downregulation of Bcl-xl and up-regulation of Bax and Bak in macrophages

Mus musculus

Tolrestat

inhibition of aldose reductase suppresses lipopolysaccharide-stimulated production of nitric oxide and over-expression of inducible nitric oxide synthase. Inhibition also prevents the lipopolysaccaride-induced apoptosis, cell cycle arrest, activation of caspase-3, downregulation of Bcl-xl and up-regulation of Bax and Bak in macrophages

Mus musculus

zopolrestat

inhibition of aldose reductase suppresses lipopolysaccharide-stimulated production of nitric oxide and over-expression of inducible nitric oxide synthase. Inhibition also prevents the lipopolysaccaride-induced apoptosis, cell cycle arrest, activation of caspase-3, downregulation of Bcl-xl and up-regulation of Bax and Bak in macrophages

Mus musculus

Source Tissue (protein specific)

Source Tissue

Commentary

Organism

Textmining

RAW-264.7 cell

inhibition or RNA interference ablation of aldose reductase suppresses lipopolysaccharide-stimulated production of nitric oxide and over-expression of inducible nitric oxide synthase. Inhibition also prevents the lipopolysaccaride-induced apoptosis, cell cycle arrest, activation of caspase-3, downregulation of Bcl-xl and up-regulation of Bax and Bak in macrophages